The Made-to-Order Savior

By Lisa Belkin

Published: July 1, 2001

Henry Strongin Goldberg was the first to arrive in Minneapolis. His parents decorated his room on the fourth floor of the Fairview-University Medical Center with his inflatable Batman chair, two Michael Jordan posters, a Fisher-Price basketball hoop and a punching bag hanging from the curtain rod over the bed. They took turns sleeping (or not) in his room for more than a month. It was too risky for his little brother to visit, but there was a playground across the courtyard, and if Henry, who was 4, stood at the window and Jack, who was 3, climbed to the top of the slide, the boys could wave to each other.

Henry had lost his hair by the time 6-year-old Molly Nash moved in down the hall on the bone-marrow transplant unit. Soon she, too, was bald. The two children had always looked alike, just as all children with this type of Fanconi anemia look alike, with their small faces and small eyes and bodies that are tiny for their age. The ''Fanconi face'' is one more reminder of the claim of the disease. Over time, Fanconi children also come to sound alike, with a deep, mechanical note in their voices, the result of the androgens they take to keep the illness at bay. Once their scalps were bare, Henry and Molly looked nearly identical. But there was one invisible difference between them -- a difference that could mean everything.

These two families, the Strongin-Goldbergs and the Nashes, had raced time, death, threats of government intervention and (although they cringe to admit it) each other, to make medical history. The best chance to save a Fanconi child is a bone-marrow transplant from a perfectly matched sibling donor. Many Fanconi parents have conceived second children to save their first, hoping that luck would bring them a match. These two couples became the first in the world not to count on luck. Using in-vitro fertilization, then using even newer technology to pick and choose from the resulting embryos, they each spent years trying to have a baby whose marrow was guaranteed to be an ideal genetic fit.

One family would succeed and one would fail. One child would receive a transplant from a perfectly matched newborn brother and the other from a less well-matched stranger. One would have an excellent chance of survival; the fate of the other was not as clear. Their parents, now friends, would find themselves together in the tiny lounge at the end of the transplant hall, waiting for the new cells to take root, sharing pizza and a pain that only they could understand.

When the rest of the world learned about the baby born to be a donor, there were questions. Is it wrong to breed a child for ''spare parts''? ethicists asked. If we can screen an embryo for tissue type, won't we one day screen for eye color or intelligence? There was talk in the news media of ''Frankenstein medicine'' and threats by Congress to ban embryo research, which had made this technique possible.

It is the kind of talk heard with every scientific breakthrough, from the first heart transplant to the first cloned sheep. We talk like this because we are both exhilarated and terrified by what we can do, and we wonder, with each step, whether we have gone too far. But though society may ask, ''How could you?'' the only question patients and families ask is, ''How could we not?''

Which is why there is virtually no medical technology yet invented that has not been used. It is human nature to do everything to save a life and just as human to agonize over everything we do. The story of Molly and Henry is the story of groundbreaking science. It is also the story of last-ditch gambles on unproven theories, of laboratory technique cobbled from instinct and desperation, of a determined researcher who sacrificed his job and more trying to help and of a frantic drive through a hurricane to deliver cells on time. In other words, it is simply the story of what it now takes, in the 21st century, to save one child.

Back at the beginning, it was Molly who arrived first. She was born on July 4, 1994, at Rose Medical Center in Denver, and from the start it was clear that something was terribly wrong. She was missing both thumbs, and her right arm was 30 percent shorter than her left. Her parents, Lisa and Jack, saw her, but could not hold her, before she was whisked off to the I.C.U., where doctors would eventually find two separate malformations of her heart. (She was also deaf in one ear, but that would not be known until later.) Lisa, wide awake and distraught at 4 a.m. in the maternity ward, made a phone call to the nearby university hospital where she worked as a neonatal I.C.U. nurse caring for babies just like this one, and asked a friend to bring her the book of malformations. Flipping from page to page, she landed on a photo of a Fanconi face and saw in it the face of her newborn daughter.

Named for the Swiss physician who first identified it in 1927, Fanconi anemia causes bone marrow failure, eventually resulting in leukemia and other forms of cancer. Until very recently, children with Molly's form of F.A. rarely lived past the age of 6, the age Molly is right now. Fanconi is a recessive disorder, which means both parents must pass along one copy of the mutated gene in order for a child to develop the disease. Among the general population, one of every 200 people has a Fanconi mutation. Every ethnic group carries its own genetic baggage, however, and among Ashkenazi Jews like the Nashes and Strongin-Goldbergs, the incidence is 1 in 89, meaning that if both parents are Ashkenazi Jews the chance of having an affected baby is 1 in 32,000. But Lisa, with all her medical training, had never heard of the disease, and Jack, a Denver hotel manager, certainly had not, either.